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Immunology Y5 > Case studies in immunology > Flashcards

Case studies in immunology Flashcards

1
Q

Basic pathophysiology of anaphylaxis

A
  • Type I hypersensitivity response
  • Previously sensitised to the allergen
  • Re-exposure → cross-linking of IgE on the surface of mast cells
  • This causes mast cells to degranulate
  • This results in the release of specific biological mediators including histamines and leukotrienes
  • This results in:
    • Increased vascular permeability
    • Smooth muscle contraction
    • Inflammation, increased mucus production
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2
Q

Common causes of anaphylaxis

A
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3
Q

Most commom features of anaphylaxis

A

Urticaria and angiooedema

followed by upper airway oedema

***usually do get skin manifestations **

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4
Q

Management of anaphylaxis

A
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5
Q

What is Latex?

A

milky fluid produced by rubber trees (Hevea brasiliensis

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6
Q

What are the two types of hypersensitivity reactions you can get with latex?

A
  1. Type 1
    - IgE mediated
    - immediate
    - cross-reactive with certain fruits (Latex fruit allergy syndrome) - BAACK
  2. Type 4
    - contact dermatitis
    - 24-48 hours after exposure
    - usually affects hands and feet
    - usually due to rubber additives rather than latex itself
    - unresponsive to antihistamines as it’s not mediated by histamine
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7
Q

Investigations for latex allergy

A
  • skin prick testing (in vivo)
  • patch testing (in vivo)

- specific IgE - preferable in patients with a history of anaphylaxis. but poor sensitivity and specificity.

- component individual allergen test: higher sensitiivty

  • challenge test - if inconclusive skin prick or blood test

Trend: skin, blood, challenge

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8
Q

What allergies does desensitisation work for?

A
  • insect venom
  • some aeor-allergens eg pollen

**not latex **

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9
Q

What disorders are associated with recurrent meningococcal meningitis?

A
  1. complement deficiency - susceptibility to encapsulated bacteria
  2. antibody deficiency- susceptibility to bacterial infections, esp. upper and lower respiratory tract

**but also neurological disorders such as skull fracture**

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10
Q

Factors that imply immunodeficiency

A
  1. Serious infections (from innocuous/ harmless organisms)
  2. Persistent infections- e.g. resistant to Abx Tx
  3. Unusual
    • Unusual organisms
    • Opportunistic organisms
    • Unusual sites of infection- deep muscle abscesses
  4. Recurrent minor infections

Concomitant problems:

  • Failure to thrive
  • Family history
  • History of autoimmune diagnosis, malignancy etc.
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11
Q

How does the CH50 test work?

A
  • CH50 is a functional test of the integrity of the whole CLASSICAL complement cascade
  • Classical pathway is activated by Ab bound to antigen
  • The CH50 test uses antibody-coated sheep RBC
  • If classical pathway is working, those RBC will be lysed
  • So you mix patient’s serum with the preparation of antibody-coated sheep RBC
  • Test measures the haemolysis by the release of Hb
  • Positive/ normal test = good amount of haemolysis
    • Note: ALL components of the cascade (classical pathway and final common pathway) need to be in place for the test
    • → membrane attack complex → haemolysis
    • → give a positive (NORMAL) result
    • Low/ absent haemolysis = immunolgical problem - complement deficiency
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12
Q

How does the AP50 test work?

A
  • AP50 is a functional test of the integrity of the whole ALTERNATIVE complement cascade
  • Uses rabbit RBC which has a coating that is not protected from complement lysis using the alternative pathway
  • Mix rabbit RBC and patient’s serum
  • If alternative pathway works → membrane attack complex → haemolysis of rabbit RBC
  • Positive result = good amount of haemolysis (normal)
  • ALL components of the cascade (alternative and final common) need to be in place for the test to give a positive (NORMAL) result
  • Low/ absent haemolysis = immunolgical problem - complement deficiency
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13
Q

NORMAL C3 and C4

Absent CH50

Absent AP50

A

Defect of final common pathway

C5, C6, C7, C8, C9

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14
Q

Why can’t you give patients complement for complement deficiency

A

because complement protein is labile

Instead- you give: vaccinations against encapuslated bacteria and daily prophylactic penicilin

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15
Q

Which immunologicla defect increases susceptibility to meningococcal disease?

A

Any complement deficiency but especially alternative pathway or final common pathway defect

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16
Q

SLE antibodies

A

Anti ds-DNA: most specific

Anti-Ro, anti-La, anti-Sm, anti-RNP: not specific

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17
Q

Limited cutaneous systemic sclerosis (CREST syndrome) antibodies

A

Anti-centromere

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18
Q

Diffuse systemic sclerosis antibody (scleroderma)

A

anti-topoisomerase - anti-SCL 70

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19
Q

Sjogren’s antibodies

A

Anti Ro

Anti La

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20
Q

Myositis antibodies

A

anti-Jo1 (type of tRNA synthetase)

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21
Q

Types of ANA antibodies

A
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22
Q

What suggests SLE is active?

A

Low C3 and C4

Also can monitor disease activity with ESR and anti-ds DNA antibody

**but need to correlate with clinical picture

23
Q

Renal biopsy of lupus nephritis vs goodpasture’s

A

Lupus nephritis: lumpy bumpy (grnaular) deposition of immune complexes

*diffuse prolfierative nephritis is the most common pattern foudn in the kidneys

Goodpastures: linear deposition of antibodies at the glomerular basement membrane

24
Q

Two main regions affected by SLE

A

joints and kidney

25
Drugs useful for treatment of SLE
26
PBC antibody
Anti-mitochondrial antibody
27
28
29
What is serum sickness?
Type III hypersensitivity (immune complex mediated) reaction to drugs like penicillin **key thing:** involves a foreign protein rather than an autoantigen as in SLE
30
Clinical manifestations of serum sickness
disorientation - because immune complexes lead to small vessel vasculitis in the blood vessels leading to the brain
31
Investigations for serum sickness
32
33
34
Investigations for immunodeficiency
**FISH** FBC Immunoglobulin Serum c3 and c4 (complement) HIV
35
CD4 and CD8 T cells – present B cells- very LOW numbers Specific responses to tetanus/ HiB- NEGATIVE
Bruton's X-linked agammaglobulinaemia
36
What is Bruton's X-linked agammaglobulinaemia
Deficiency of a tyrosine kinase needed for B lymphocyte maturation from bone marrow going out into circulation Failure of pre-B cells to mature in the bone marrow → low B cell numbers This leads to failure to produce immunoglobulins → Low Ab numbers
37
Mx of bruton's
* pooled serum Ig * HSCT
38
What is flow cytometry used for in. the context of immunodeficiency investgation?
To test for lymphoid markers to figure out which subset it is
39
Bruton's x linked agammaglobulinaemia
40
Ddx?
Multiple myeloma (top differential) Osteoporosis and Sjogren’s syndrome Osteoporosis and SLE **\*\*\*rmb, you can get recurrent infections in multiple myeloma because of bone marrow infiltration\*\*\***
41
What region of antibody determines class of antibody?
heavy chain \*\*light chain determines the specificty for diff antigens as it's found in the antigen binding region
42
Multiple myeloma tests
**1. serum imuunoglobulins** **2. serum protein electrophoresis** - looking at HEAVY chain to see whether monoclonal band - can be negative **3. urinary bence jones protein** - looking at LIGHT chain - need to do this because in 75% of patients with MM you don't get monoclonal band on serum electrophoresis (4) x-ray : punched out lytic lesions
43
Why do you get recurrent infections in multiple myeloma? Why do you get anaemia in multiple myeloma? Why is ESR raised?
**Recurrent infections** * there's suppression of normal immunoglobulin by the malignant clone * → results in a functional antibody deficiency * This is sometimes called immune paresis **Anaemia** * Expansion of malignant clone of plasma cells * → crowds out the normal RBC and WBC precursors in the bone marrow * The tumour may produce local cytokines which inhibits normal bone marrow function **Raised ESR** * ESR = measure of the rate of fall of erythrocytes through plasma * Normally, erythrocytes do NOT clump * because the repellent negative surface charge is greater than the attractant charge of plasma constituents * However, if the protein constituents of plasma increase/ change: * Increases attractant charge * Causes erythrocytes to clump together * Clumped erythrocytes fall more quickly * This results in a raised ESR
44
ESR and CRP in rheumatoid arthritis and SLE
RA: ESR and CRP both raised SLE: ESR raised, CRP normal
45
RF antibodies
RF Anti-CCP- specific
46
What is a common trigger for rheumatoid arthritis?
Post-partum presentation is common Due to change in T-cell phenotype from Th2 to Th1 after delivery
47
What is Rheumatoid Factor? Why is it not diagnostic of rheumatoid arthritis?
IgM (usually) antibodies are directed against the Fc region of human IgG * Assays look for the IgM RF although patients may also have IgG and IgA RF * RF is not very specific to Rheumatoid Arthritis * Approximately 60-70% sensitive and specific (found in other diseases)
48
49
Genetic associations of rheumatoid arthritis
1. **HLA associations** HLA DR1 HLA DR 4 2. **PAD Type 2 and 4** 3. **PTPN22**
50
Management of rheumatoid arthritis
TNF alpha antagonists- infliximab, etanercept
51
Name an anti CTLA4 agent
Abatacept
52
Pathognemonic features of rhematoid arthritis
synovitis
53
Key cytokines in rheumatoid arthritis - targeted by drugs
1. IL6 2. TNF Alpha - produced by macrophages (IL1 is another minor cytokine)

Immunology Y5 (11 decks)

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